Pocket guide and toolkit to dejongs neurologic examination

Authors: Campbell, William W.
Title: Pocket Guide and Toolkit to DeJong's Neurologic Examination, 1st Edition
Copyright ©2008 Lippincott Williams & Wilkins
> Fr ont of Book > Author s
Authors
William W. Campbell MD, MSHA
Professor and Chairman
Department of Neurology
Uniformed Services University of Health Sciences
Bethesda, Maryland
Chief, Clinical Neurophysiology
Walter Reed Army Medical Center
Washington, DC
Authors: Campbell, William W.
Title: Pocket Guide and Toolkit to DeJong's Neurologic Examination, 1st Edition
Copyright ©2008 Lippincott Williams & Wilkins
> Fr ont of Book > Dedication
Dedication
To Wes, Matt and Shannon; to Russell N. DeJong, neurologist extraordinaire; and to Anne Sydor.
Authors: Campbell, William W.
Title: Pocket Guide and Toolkit to DeJong's Neurologic Examination, 1st Edition
Copyright ©2008 Lippincott Williams & Wilkins
> Table of Contents > Section A - Intr oduction > Chapter 1 - Intr oduction
Chapter 1
Introduction
This book is written as a companion and supplement to DeJong's The Neurologic Examination, 6
th

edition. The book has been streamlined,
all reference to basic science removed, and the essentials of the clinical examination presented. In addition, novel to medical books as far
as I am aware, there are appendices (a “Toolkit”) that contain some commonly used and handy instruments and forms that are often useful
in the examination of the neurologic patient, especially in regard to neuroophthalmology. These include: a simple red lens for diplopia
testing, a multi-pinhole for assessing visual acuity, pocket vision screeners for examining near visual acuity at near and at a distance of
about 6 feet, a primitive but usable version of an OKN tape, 4 red squares with dots to assess color vision in all 4 quadrants, selected color
vision plates, an Amsler grid for evaluating central scotomas, a copy of the Blessed memory-orientation questionnaire, and copies of the
Glasgow coma scale, the Hunt and Hess scale for evaluating subarachnoid hemorrhage patients, and a diagram of the brachial plexus.
Commercial interests would not allow the inclusion of the Folstein mini-mental examination.
The hope is that the Toolkit will elevate the Pocket Guide from a mere abbreviated textbook on the neurologic examination to a useful
clinical tool for examining patients. With the Pocket Guide and its accompanying Tools, along with the usual instruments found in the
neurologist's black bag, the examiner should find at hand all the reasonable tools with which to do a complete neurologic examination, to
include detailed neuro-ophthalmologic assessment.
The larger textbook, DeJong's The Neurologic Examination, remains the definitive source for all aspects, common and abstruse, for a
discussion of the examination. The Pocket Guide is intended as a brief version, pocket or bag portable, that contains the essentials of the
examination as well as many of the tools that are often hard to find when needed most.
NEUROLOGIC DIFFERENTIAL DIAGNOSIS
Pathologic processes behave in certain ways depending on their location in the nervous system, and in certain other ways related to their
inherent natures. Neurologists deal in two basic clinical exercises: where is the lesion in the nervous system and what is the lesion in the
nervous system: differential diagnosis by location and differential diagnosis by pathophysiology or etiology. The anatomic diagnosis and the
etiologic diagnosis aid and support each other. In general, the neurologic examination aids primarily in establishing the anatomic or
localization diagnosis and the history aids in the etiologic diagnosis, but there is overlap. The examination also serves to indicate the
severity of the abnormality. A dependence on neuro-imaging and other tests as the primary approach to diagnosis causes many errors.
Defining the patient's illness first in terms of anatomy and likely etiology helps insure the appropriate use of neurodiagnostic studies.
The first consideration should be whether the patient has an organic disease or whether the symptoms are likely psychogenic. If the
disorder is organic, consider whether the condition is a primary neurologic disease, a neurologic complication of a systemic disorder, a
neurologic complication of drug or medication use, or the effects of a toxin.
ANATOMICAL DIAGNOSIS
The patterns of abnormality found on examination help to localize a disease process to a particular part of the nervous system. Clinical
features that are particularly helpful in neurologic differential diagnosis include the distribution of any weakness, the presence or absence

of sensory symptoms, the presence or absence of pain, the presence or absence of cranial nerve abnormalities and whether they are
ipsilateral or contralateral to the other abnormalities on examination, the status of the reflexes, the presence of pathological reflexes,
involvement of bowel and bladder function, and the presence or absence of symptoms that clearly indicate cortical involvement. Weakness
may be unilateral or bilateral, symmetric or asymmetric, primarily proximal or primarily distal; each of these patterns has differential
diagnostic significance. The pattern of sensory abnormalities also provides significant information.
In trying to make an anatomical localization, it may be helpful to organize the nervous system by considering sequentially more peripheral
or central structures, beginning either at the cerebral cortex or the muscle. Consider each level where disease tends to have a
characteristic and reproducible clinical profile. For example, disease involving the muscle, neuromuscular junction, peripheral nervous
system, nerve roots, spinal cord, brainstem, and hemispheres each tend to produce a characteristic clinical picture. Some diseases cause
multifocal or diffuse abnormalities, and these are often particularly challenging.
At each major level, disease processes tend to have characteristic clinical features, although with some degree of overlap. By trying to
localize the disease process to one or two likely levels, such as muscle or neuromuscular junction, one can then think more systematically
about the etiologic possibilities.
MUSCLE DISEASE
Common muscle diseases include muscular dystrophies and inflammatory, metabolic, toxic, and congenital myopathies. Patients with muscle
disease usually have symmetric, proximal weakness. Deep tendon reflexes (DTRs) are usually intact but may be depressed when weakness is
severe. There are no pathological reflexes. Patients may or may not have muscle pain, tenderness or soreness; usually they do not. There
is no sensory loss; bowel and bladder dysfunction generally do not occur, there are no defects in coordination, mentation, or higher
cortical function.
NEUROMUSCULAR JUNCTION (NMJ) DISORDERS
NMJ diseases include myasthenia gravis (MG), Lambert-Eaton syndrome, botulism, hypermagnesemia, and others. The most common
condition by far is M G. Patients with NM J disorders usually
have symmetric, proximal muscle weakness, which can simulate a myopathy, but in addition often have bulbar involvement. M ost commonly
patients have weakness of eye movement causing double vision, or ptosis of one or both eyelids. They may have trouble talking and
swallowing, with a tendency to nasal regurgitation of fluids. Such symptoms and signs of bulbar weakness are one of the main differences
between an NMJ disease and a myopathy. There is no pain or sensory loss. DTRs are normal in M G but may be depressed in Lambert-Eaton
syndrome and other presynaptic disorders. There are no pathological reflexes.
PERIPHERAL NEUROPATHY
Common causes of peripheral neuropathy include diabetes mellitus, alcoholism, and GBS. M ost patients with polyneuropathy have
symmetric, predominantly distal weakness, sensory loss, depressed or absent DTRs, no pathologic reflexes, and no bowel or bladder

dysfunction. Pain is a common accompaniment and often a major clinical feature. Proximal weakness can occur with some neuropathies.
PLEXUS DISEASE
Diseases involving the brachial plexus are much more common than those involving the lumbosacral plexus. M ost brachial plexopathies are
due to trauma. Neuralgic amyotrophy (brachial plexitis, Parsonage-Turner syndrome) is a common inflammatory disorder of the brachial
plexus that is notoriously painful. Patients with plexus disorders have a clinical deficit which mirrors the involved structures, so a
knowledge of plexus anatomy is vital to deciphering the deficit. There is typically both weakness and sensory loss, accompanied by
depressed or absent DTRs in the involved area, no pathologic reflexes, and no bowel or bladder dysfunction.
NERVE ROOT DISEASE
Most radiculopathies are due to disc herniations or spondylosis. When severe, there are both motor and sensory deficits and a depressed
DTR in the distribution of the involved root(s). Pain is common and often severe, usually accompanied limitation of motion of either the
neck or lower back, along with signs of root irritability, such as a positive straight leg raising test. There are no pathological reflexes, and
no bowel or bladder dysfunction. The presence of these findings suggests there is concomitant spinal cord compression.
SPINAL CORD DISEASE
Common causes of myelopathy include compression, trauma, and acute transverse myelitis. With transverse myelopathy, there is symmetric
involvement causing bilateral weakness below a particular level, producing either paraparesis or quadriparesis. In addition to weakness
below the level of the lesion, patients with spinal cord lesions may also have paresthesias, numbness, tingling, and sensory loss with a
discrete sensory level, usually on the trunk. Except during the acute phase, patients with spinal cord disease tend to have increased
reflexes, along with pathologic reflexes such as the Babinski sign. Patients with spinal cord disease also tend to have difficulty with
sphincter control, and bladder dysfunction is often an early and prominent symptom. Pain is not a common feature except for local
discomfort due to a vertebral lesion. Peripheral neuropathy may also cause symmetric motor and sensory loss, but DTRs are decreased,
sphincter dysfunction is very rare, and there is often pain.
BRAINSTEM DISEASE
The classic distinguishing feature of brainstem pathology is that deficits are “crossed,” with cranial nerve dysfunction on one side and a
motor or sensory deficit on the opposite side. There are often symptoms reflecting dysfunction of other posterior fossa structures, such
as vertigo, ataxia, dysphagia, nausea and vomiting, and abnormal eye movements. Unless the process has impaired
the reticular activating system, patients are normal mentally, awake, alert, able to converse (though perhaps dysarthric), not confused,
and not aphasic. DTRs are usually hyperactive with accompanying pathologic reflexes in the involved extremities; pain is rare and sphincter
dysfunction occurs only if there is bilateral involvement.
CRANIAL NERVE DISEASE
Disease may selectively involve one, or occasionally more than one, cranial nerve. The long tract abnormalities, vertigo, ataxia, and similar

symptoms and findings that are otherwise characteristic of intrinsic brainstem disease are lacking. Common cranial neuropathies include
optic neuropathy due to multiple sclerosis, third nerve palsy due to aneurysm, and Bell palsy. Involvement of more than one nerve occurs
in conditions such as Lyme disease, sarcoidosis, and lesions involving the cavernous sinus.
CEREBELLAR DISEASE
Patients with cerebellar dysfunction suffer from various combinations of tremor, incoordination, difficulty walking, dysarthria and
nystagmus, depending on the parts of the cerebellum involved. There is no weakness, sensory loss, pain, hyperreflexia, pathologic reflexes,
sphincter dyscontrol, or abnormalities of higher cortical function. When cerebellar abnormalities result from dysfunction of the cerebellar
connections in the brainstem there are usually other brainstem signs.
BASAL GANGLIA DISORDERS
Diseases of the basal ganglia cause movement disorders such as Parkinson disease or Huntington chorea. Movement disorders may be
hypokinetic or hyperkinetic, referring to whether movement is in general decreased or increased. Parkinson disease causes bradykinesia
and rigidity. Huntington disease in contrast causes increased movements that are involuntary and beyond the patient's control (chorea).
Tremor is a frequent accompaniment of basal ganglia disease.
CEREBRAL HEMISPHERE DISORDERS, CORTICAL V. SUBCORTICAL
Characteristic of unilateral hemispheric pathology is a “hemi” deficit: hemisensory loss, hemiparesis, hemi-anopsia, or perhaps
hemiseizures. Other common manifestations include hyperreflexia and pathologic reflexes. Pain is not a feature unless the thalamus is
involved, and there is no difficulty with sphincter control unless both hemispheres are involved. Within this framework, disease affecting
the cerebral cortex behaves differently from disease of subcortical structures. Patients with cortical involvement may have aphasia,
apraxia, astereognosis, impaired two point discrimination, memory loss, cognitive defects, focal seizures, or other abnormalities that
reflect the essential integrative role of the cortex. Processes affecting the dominant hemisphere often cause language dysfunction in the
form of aphasia, alexia, or agraphia. With disease of the non-dominant hemisphere, the patient may have higher cortical function
disturbances involving functions other than language, such as apraxia. If the disease affects subcortical structures, the clinical picture
includes the hemidistribution of dysfunction but lacks those elements that are typically cortical, e.g., language disturbance, apraxia,
seizures, dementia.
MULTIFOCAL/DIFFUSE DISORDERS
Some disease processes are diffuse or multifocal, producing dysfunction at more than one location, or involve a “system.” For example,
Devic disease characteristically affects both the spinal cord and the optic nerves, i.e., it is multifocal. ALS is a system disorder causing
diffuse dysfunction of the entire motor system from the spinal cord to the cerebral cortex, sparing sensation and higher cortical function.
DIFFERENTIAL DIAGNOSIS BY ETIOLOGY
From a differential diagnostic standpoint, it is usually most helpful to think first about the localization of the disease process in the nervous

system, and secondarily about the etiology. Localization limits the etiologic differential diagnosis, since certain disease processes typically
involve or spare particular structures. Knowing the likely location of the pathology generally places the condition into a broad etiologic
differential diagnostic category. Occasionally, the etiology is very obvious, such as stroke or CNS trauma and the diagnostic exercise
focuses mostly on the localization. Some of the etiologies of primary neurologic disease include neoplasms, vascular disease, infection,
inflammation, autoimmune disorders, trauma, toxins, substance abuse, metabolic disorders, demyelinating disease, congenital abnormalities,
migraine, epilepsy, genetic and degenerative conditions. Neurologic complications of systemic disease are very common.
Psychiatric disease as an etiologic category requires a caveat. The psychiatric disorders most often of neurologic concern are depression,
hysteria, malingering, and hypochondriasis. These are also frequently referred to as functional or nonorganic disorders. Depression tends
to exaggerate any symptomatology, neurologic or otherwise. The diagnosis of nonorganic disease can be treacherous. So-called “hysterical
signs” on physical examination are often extremely misleading.
Authors: Campbell, William W.
Title: Pocket Guide and Toolkit to DeJong's Neurologic Examination, 1st Edition
Copyright ©2008 Lippincott Williams & Wilkins
> Table of Contents > Section B - Histor y, Physical Ex amination, and Over view of the Neur ologic Ex amination > Chapter 2 - The Neur ologic Histor y
Chapter 2
The Neurologic History
Introductory textbooks of physical diagnosis cover the basic aspects of medical interviewing. This chapter addresses some aspects of
history taking of particular relevance to neurologic patients. Important historical points to be explored in some common neurologic
conditions are summarized in the tables.
The history is the cornerstone of medical diagnosis, and neurologic diagnosis is no exception. In many instances the physician can learn
more from what the patient says and how he says it than from any other avenue of inquiry. A skillfully taken history will frequently indicate
the probable diagnosis, even before physical, neurologic, and neurodiagnostic examinations are carried out. Conversely, many errors in
diagnosis are due to incomplete or inaccurate histories. In many common neurologic disorders the diagnosis rests almost entirely on the
history. The most important aspect of history taking is attentive listening. Ask open ended questions and avoid suggesting possible
responses. Although patients are frequently accused of being “poor historians,” there are in fact as many poor history takers as there are
poor history givers. While the principal objective of the history is to acquire pertinent clinical data that will lead to correct diagnosis, the
information
obtained in the history is also valuable in understanding the patient as an individual, his relationship to others, and his reactions to his
disease.
Taking a good history is not simple. It may require more skill and experience than performing a good neurologic examination. Time,

diplomacy, kindness, patience, reserve, and a manner that conveys interest, understanding, and sympathy are all essential. The physician
should present a friendly and courteous attitude, center all his attention on the patient, appear anxious to help, word questions tactfully,
and ask them in a conversational tone. At the beginning of the interview it is worthwhile to attempt to put the patient at ease. Avoid any
appearance of haste. Engage in some small talk. Inquiring as to where the patient is from and what they do for a living not only helps make
the encounter less rigid and formal, but often reveals very interesting things about the patient as a person. History taking is an
opportunity to establish a favorable patient-physician relationship; the physician may acquire empathy for the patient, establish rapport,
and instill confidence. The manner of presenting his history reflects the intelligence, powers of observation, attention, and memory of the
patient. The examiner should avoid forming a judgment about the patient's illness too quickly; some individuals easily sense and resent a
physician's preconceived ideas about their symptoms. Repeating key points of the history back to the patient helps insure accuracy and
assure the patient the physician has heard and assimilated the story. At the end of the history, the patient should always feel as if he has
been listened to. History taking is an art; it can be learned partly through reading and study, but is honed only through experience and
practice.
The mode of questioning may vary with the age and educational and cultural background of the patient. The physician should meet the
patient on a common ground of language and vocabulary, resorting to the vernacular if necessary, but without talking down to the
patient. This is sometimes a fine line. The history is best taken in private, with the patient comfortable and at ease.
The history should be recorded clearly and concisely, in a logical, well-organized manner. It is important to focus on the more important
aspects and keep irrelevancies to a minimum; the essential factual material must be separated from the extraneous. Diagnosis involves the
careful sifting of evidence, and the art of selecting and emphasizing the pertinent data may make it possible to arrive at a correct
conclusion in a seemingly complicated case. Recording negative as well as positive statements assures later examiners that the historian
inquired into and did not overlook certain aspects of the disease.
Several different types of information may be obtained during the initial encounter. There is direct information from the patient describing
the symptoms, information from the patient regarding what previous physicians may have thought, and information from medical records or
previous care givers. All these are potentially important. Usually, the most essential is the patient's direct description of the symptoms.
Always work from information obtained firsthand from the patient when possible, as forming one's own opinion from primary data is critical.
Steer the patient away from a description of what previous doctors have thought, at least initially. M any patients tend to jump quickly to
describing encounters with caregivers, glossing over the details of the present illness. Patients often misunderstand much or most of what
they have been told in the past, so information from the patient about past evaluations and treatment must be analyzed cautiously. Patient
recollections may be flawed because of faulty memory, misunderstanding, or other factors. Encourage the patient to focus on symptoms
instead, giving a detailed account of the illness in his own words.
In general, the interviewer should intervene as little as possible, but it is often necessary to lead the conversation away from obviously

irrelevant material, obtain amplification on vague or incomplete statements, or lead the story in directions likely to yield useful
information. Allow the patient to use his own words as much as possible, but it is important to determine the precise meaning of words
the patient uses, clarifying any ambiguity that could lead to misinterpretation. Have the patient clarify what he means by lay terms like
“kidney trouble” or “dizziness.”
Deciding whether the physician or the patient should control the pace and content of the interview is a frequent problem. Patients do
not practice history giving. Some are naturally much better
at relating the pertinent information than others. M any patients digress frequently into extraneous detail. The physician adopting an
overly passive role under such circumstances often prolongs the interview unnecessarily. When possible, let the patient give the initial
part of the history without interruption. In a primary care setting, the average patient tells his story in about five minutes. The average
doctor interrupts the average patient after only about 18 seconds. In 44% of interviews done by medical interns, the patient was not
allowed to complete their opening statement of concerns. Female physicians allowed fewer patients to finish their opening statement.
Avoid interrogation, but keeping the patient on track with focused questions is entirely appropriate. If the patient pauses to remember
some irrelevancy, gently encourage them not to dwell on it. A reasonable method is to let the patient run as long as they are giving a
decent account, then take more control to clarify necessary details. Some patients may need to relinquish more control than others.
Experienced clinicians generally make a diagnosis through a process of hypothesis testing. At some point in the interview, the physician
must assume greater control and query the patient regarding specific details of their symptomatology in order to test hypotheses and help
to rule in or rule out diagnostic possibilities.
History taking in certain types of patients may require special techniques. The timid, inarticulate, or worried patient may require
prompting with sympathetic questions or reassuring comments. The garrulous person may need to be stopped before getting lost in a mass
of irrelevant detail. The evasive or undependable patient may have to be queried more searchingly, and the fearful, antagonistic, or
paranoid patient questioned guardedly to avoid arousing fears or suspicions. In the patient with multiple or vague complaints, insist on
specifics. The euphoric patient may minimize or neglect his symptoms; the depressed or anxious patient may exaggerate, and the excitable
or hypochondriacal patient may be overconcerned and recount his complaints at length. The range of individual variations is wide, and this
must be taken into account in appraising symptoms. What is pain to the anxious or depressed patient may be but a minor discomfort to
another. A blasé attitude or seeming indifference may indicate pathologic euphoria in one individual, but be a defense reaction in
another. One person may take offense at questions which another would consider commonplace. Even in a single individual such factors as
fatigue, pain, emotional conflicts, or diurnal fluctuations in mood or temperament may cause a wide range of variation in response to
questions. Patients may occasionally conceal important information. In some cases, they may not realize the information is important; in
other cases, they may be too embarrassed to reveal certain details.
The interview provides an opportunity to study the patient's manner, attitude, behavior, and emotional reactions. The tone of voice,

bearing, expression of the eyes, swift play of facial muscles, appearance of weeping or smiling, or the presence of pallor, blushing,
sweating, patches of erythema on the neck, furrowing of the brows, drawing of the lips, clenching of the teeth, pupillary dilation, or
muscle rigidity may give important information. Gesticulations, restlessness, delay, hesitancy, and the relation of demeanor and emotional
responses to descriptions of symptoms or to details in the family or marital history should be noted and recorded. These and the mode of
response to the questions are valuable in judging character, personality, and emotional state.
The patient's story may not be entirely correct or complete. He may not possess full or detailed information regarding his illness, may
misinterpret his symptoms or give someone else's interpretation of them, wishfully alter or withhold information, or even deliberately
prevaricate for some purpose. The patient may be a phlegmatic, insensitive individual who does not comprehend the significance of his
symptoms, a garrulous person who cannot give a relevant or coherent story, or have multiple or vague complaints that cannot be readily
articulated. Infants, young children, comatose or confused patients may be unable to give any history. Patients who are in pain or distress,
have difficulty with speech or expression, are of low intelligence, or do not speak the examiner's language are often unable to give a
satisfactory history for themselves. Patients with nondominant parietal lesions are often not fully aware of the extent of their deficit. It
may be necessary to corroborate or supplement
the history given by the patient by talking with an observer, relative, or friend, or even to obtain the entire history from someone else.
Family members may be able to give important information about changes in behavior, memory, hearing, vision, speech, or coordination of
which the patient may not be aware. It is frequently necessary to question both the patient and others in order to obtain a complete
account of the illness. Family members and significant others sometimes accompany the patient during the interview. They can frequently
provide important supplementary information. However, the family member must not be permitted to dominate the patient's account of
the illness unless the patient is incapable of giving a history.
It is usually best to see the patient de novo with minimal prior review of the medical records. Too much information in advance of the
patient encounter may bias one's opinion. If it later turns out that previous caregivers reached similar conclusions based on primary
information, this reinforces the likelihood of a correct diagnosis. So, see the patient first, review old records later.
There are three approaches to utilizing information from past caregivers, whether from medical records or as relayed by the patient. In
the first instance, the physician takes too much at face value and assumes that previous diagnoses must be correct. An opposite approach,
actually used by some, is to assume all previous caregivers were incompetent, and their conclusions could not possibly be correct. This
approach sometimes forces the extreme skeptic into a position of having to make some other diagnosis, even when the preponderance of
the evidence indicates that previous physicians were correct. The logical middle ground is to make no assumptions regarding the opinions
of previous caregivers. Use the information appropriately, matching it against what the patient relates and whatever other information is
available. Do not unquestioningly believe it all, but do not perfunctorily dismiss it either. Discourage patients from grousing about their
past medical care and avoid disparaging remarks about other physicians the patient may have seen. An accurate and detailed record of

events in cases involving compensation and medicolegal problems is particularly important.
One efficient way to work is to combine reviewing past notes with talking directly with the patient. If the record contains a reasonably
complete history, review it with the patient for accuracy. For instance, read from the record and say to the patient, “Dr. Payne says here
that you have been having pain in the left leg for the past 6 months. Is that correct?” The patient might verify that information, or may say,
“No, it's the right leg and it's more like 6 years.” Such an approach can save considerable time when dealing with a patient who carries
extensive previous records. A very useful method for summarizing a past workup is to make a table with two vertical columns, listing all
tests which were done, with those that were normal in one column and those that were abnormal in the other column.
Many physicians find it useful to take notes during the interview. Contemporaneous note taking helps insure accuracy of the final report.
A useful approach is simply to “take dictation” as the patient talks, particularly in the early stages of the encounter. A note sprinkled with
patient quotations is often very illuminating. However, one must not be fixated on note taking. The trick is to interact with the patient,
and take notes unobtrusively. The patient must not be left with the impression that the physician is paying attention to the note taking
and not to them. Such notes are typically used for later transcription into some final format. Sometimes the patient comes armed with
notes. The patient who has multiple complaints written on a scrap of paper is said to have la maladie du petit papier; tech savvy patients
may come with computer printouts detailing their medical histories.
THE PRESENTING COMPLAINT AND THE PRESENT ILLNESS
The neurologic history usually starts with obtaining the usual demographic data, but must also include handedness. The traditional
approach to history taking begins with the chief complaint and present illness. In fact, many experienced clinicians begin with the
pertinent past history, identifying major underlying past or chronic medical illnesses at the outset. This does not mean going into detail
about unrelated past surgical procedures and the like. It does mean identifying major
comorbidities which might have a direct or indirect bearing on the present illness. This technique helps to put the present illness in
context and to prompt early consideration about whether the neurologic problem is a complication of some underlying condition or an
independent process. It is inefficient to go through a long and laborious history in a patient with peripheral neuropathy, only to
subsequently find out in the past history that the patient has known, long standing diabetes.
While a complete database is important, it is counterproductive to give short shrift to the details of the present illness. History taking
should concentrate on the details of the presenting complaint. The majority of the time spent with a new patient should be devoted to
the history and the majority of the history taking time should be devoted to the symptoms of the present illness. The answer most often
lies in the details of the presenting problem. Begin with an open ended question, such as, “what sort of problems are you having?” Asking
“what brought you here today?” often produces responses regarding a mode of transportation. And asking “what is wrong with you?” only
invites wisecracks. After establishing the chief complaint or reason for the referral, make the patient start at the beginning of the story
and go through more or less chronologically. M any patients will not do this unless so directed. The period of time leading up to the onset

of symptoms should be dissected to uncover such things as the immunization that precipitated an episode of neuralgic amyotrophy, the
diarrheal illness prior to an episode of Guillain-Barre syndrome, or the camping trip that lead to the tick bite. Patients are quick to assume
that some recent event is the cause for their current difficulty. The physician must avoid the trap of assuming that temporal relationships
prove etiologic relationships.
Record the chief complaint in the patient's own words. It is important to clarify important elements of the history that the patient is
unlikely to spontaneously describe. Each symptom of the present illness should be analyzed systematically by asking the patient a series of
questions to clear up any ambiguities. Determine exactly when the symptoms began, whether they are present constantly or
intermittently, and if intermittently the character, duration, frequency, severity, and relationship to external factors. Determine the
progression or regression of each symptom, whether there is any seasonal, diurnal, or nocturnal variability, and the response to
treatment. In patients whose primary complaint is pain, determine the location; character or quality; severity; associated symptoms; and, if
episodic, frequency, duration, and any specific precipitating or relieving factors. Some patients have difficulty describing such things as
the character of a pain. Although spontaneous descriptions have more value, and leading questions should in general be avoided, it is
perfectly permissible when necessary to offer possible choices, such as “dull like a toothache” or “sharp like a knife.”
In neurologic patients, particular attention should be paid to determining the time course of the illness, as this is often instrumental in
determining the etiology. An illness might be static, remittent, intermittent, progressive, or improving. Abrupt onset followed by
improvement with variable degrees of recovery are characteristic of trauma and vascular events. Degenerative diseases have a gradual
onset of symptoms and variable rate of progression. Tumors have a gradual onset and steady progression of symptoms, with the rate of
progression depending on the tumor type. With some neoplasms hemorrhage or spontaneous necrosis may cause sudden onset or
worsening. M ultiple sclerosis is most often characterized by remissions and exacerbations, but with a progressive increase in the severity
of symptoms; stationary, intermittent, and chronic progressive forms also occur. Infections usually have a relatively sudden, but not
precipitous, onset followed by gradual improvement, and either complete or incomplete recovery. In many conditions symptoms appear
some time before striking physical signs of disease are evident, and before neurodiagnostic testing detects significant abnormalities. It is
important to know the major milestones of an illness: when the patient last considered himself to be well, when he had to stop work,
when he began to use an assistive device, when he was forced to take to his bed. It is often useful to ascertain exactly how and how
severely the patient considers himself disabled, as well as what crystallized the decision to seek medical care.
A careful history may uncover previous events which the patient may have forgotten or may not attach significance to. A history
consistent with past vascular events, trauma or episodes of demyelination may shed entirely new light on the current symptoms. In the
patient with symptoms of myelopathy, the episode of visual loss that occurred five years previously suddenly takes on a different meaning.
It is useful at some point to ask the patient what is worrying him. It occasionally turns out that the patient is very concerned over the
possibility of some disorder that has not even occurred to the physician to consider. Patients with neurologic complaints are often

apprehensive about having some dreadful disease, such as a brain tumor, ALS, multiple sclerosis, or muscular dystrophy. All these
conditions are well known to the lay public, and patients or family members occasionally jump to outlandish conclusions about the cause
of some symptom. Simple reassurance is occasionally all that is necessary.
THE PAST MEDICAL HISTORY
The past history is important because neurologic symptoms may be related to systemic diseases. Relevant information includes a statement
about general health; history of current, chronic, and past illnesses; hospitalizations; operations; accidents or injuries, particularly head
trauma; infectious diseases; venereal diseases; congenital defects; diet; and sleeping patterns. Inquiry should be made about allergies and
other drug reactions. Certain situations and comorbid conditions are of particular concern in the patient with neurologic symptomotology.
The vegetarian or person with a history of gastric surgery or inflammatory bowel disease is at risk of developing vitamin B
12
deficiency, and
the neurologic complications of connective tissue disorders, diabetes, thyroid disease, and sarcoidosis are protean. A history of cancer
raises concern about metastatic disease as well as paraneoplastic syndromes. A history of valvular heart disease or recent myocardial
infarction may be relevant in the patient with cerebrovascular disease. In some instances, even in an adult, a history of the patient's birth
and early development is pertinent, including any complications of pregnancy, labor and delivery, birth trauma, birth weight, postnatal
illness, health and development during childhood, convulsions with fever, learning ability and school performance,
A survey of current medications, both prescribed and over the counter, is always important. M any drugs have significant neurologic side
effects. For example, confusion may develop in an elderly patient simply from the use of beta blocker ophthalmic solution; nonsteroidal
anti-inflammatory drugs can cause aseptic meningitis; many drugs may cause dizziness, cramps, paresthesias, headache, weakness, and
other side effects; and headaches are the most common side effect of proton pump inhibitors. Going over the details of the drug regimen
may reveal that the patient is not taking a medication as intended. Pointed questions are often necessary to get at the issue of over the
counter drugs, as many patients do not consider these as medicines. Occasional patients develop significant neurologic side effects from
their well-intended vitamin regimen. Patients will take medicines from alternative health care practitioners or from a health food store,
assuming these agents are safe because they are “natural,” which is not always the case. Having the patient bring in all medication bottles,
prescribed and over the counter, is occasionally fruitful.
THE FAMILY HISTORY
The family history (FH) is essentially an inquiry into the possibility of heredofamilial disorders, and focuses on the patient's lineage; it is
occasionally quite important in neurologic patients. Information about the nuclear family is also often relevant to the social history (see
below). In addition to the usual questions about cancer, diabetes, hypertension, and cardiovascular disease, the FH is particularly relevant
in patients with migraine, epilepsy, cerebrovascular disease, movement disorders, myopathy, and cerebellar disease, to list a few. In some

patients, it is pertinent to inquire
about a FH of alcoholism or other types of substance abuse. Family size is important. A negative FH is more reassuring in a patient with
several siblings and a large extended family than in a patient with no siblings and few known relatives. It is not uncommon to encounter
patients who were adopted and have no knowledge of their biological family.
There are traps, and a negative FH is not always really negative. Some diseases may be rampant in a kindred without any awareness of it by
the affected individuals. With Charcot-Marie-Tooth disease, for example, so many family members may have the condition that the pes
cavus and stork leg deformities are not recognized as abnormal. Chronic, disabling neurologic conditions in a family member may be
attributed to another cause, such as “arthritis.” Sometimes, family members deliberately withhold information about a known familial
condition.
It is sometimes necessary to inquire about the relationship between the parents, exploring the possibility of consanguinity. In some
situations, it is important to probe the patient's ethnic background, given the tendency of some neurologic disorders to occur in
particular ethnic groups or in patients from certain geographic regions.
SOCIAL HISTORY
The social history includes such things as the patient's marital status, educational level, occupation, and personal habits. The marital
history should include the number of marriages, duration of present marriage, and health of the partner and children. At times it may be
necessary to delve into marital adjustment and health of the relationship as well as the circumstances leading to any changes in marital
status.
A question about the nature of the patient's work is routine. A detailed occupational history, occasionally necessary, should delve into
both present and past occupations, with special reference to contact with neurotoxins, use of personal protective equipment, working
environment, levels of exertion and repetitive motion activities, and co-worker illnesses. A record of frequent job changes or a poor work
history may be important. If the patient is no longer working, determine when and why he stopped. In some situations, it is relevant to
inquire about hobbies and avocations, particularly when toxin exposure or a repetitive motion injury is a diagnostic consideration. Previous
residences, especially in the tropics or in areas where certain diseases are endemic, may be relevant.
A history of personal habits is important, with special reference to the use of alcohol, tobacco, drugs, coffee, tea, soft drinks and similar
substances, or the reasons for abstinence. Patients are often not forthcoming about the use of alcohol and street drugs, especially those
with something to hide. Answers may range from mildly disingenuous to bald-faced lies. Drugs and alcohol are sometimes a factor in the
most seemingly unlikely circumstances. Patients notoriously underreport the amount of alcohol they consume; a commonly used heuristic
is to double the admitted amount. To get a more realistic idea about the impact of alcohol on the patient's life the CAGE questionnaire is
useful (Table 2.1). Even one positive response is suspicious; four are diagnostic of alcohol abuse. The HALT and BUM P are other similar
question sets (Table 2.1). Some patients will not admit to drinking “alcohol” and will only confess when the examiner hits on their specific

beverage of choice, e.g., gin. Always ask the patient who denies drinking at all some follow-up question: why he doesn't drink, if he ever
drank, or when he quit. This may uncover a past or family history of substance abuse, or the patient may admit he quit only the week
before. In the patient suspected of alcohol abuse, take a dietary history.
Patients are even more secretive about drug habits. Tactful opening questions might be to ask whether the patient has ever used drugs
for other than medicinal purposes, ever abused prescription drugs, or ever ingested drugs other than by mouth. The vernacular is often
necessary: patients understand “smoke crack” better than “inhale cocaine.” It is useful to know the street names of commonly abused
drugs, but these change frequently as both slang and drugs go in and out of fashion. A less refined type of substance abuse is to inhale
common substances, such as spray
paint, airplane glue, paint thinner, and gasoline. It is astounding what some individuals will do. One patient was fond of smoking marijuana
and inhaling gasoline, leaded specifically, so that he could hallucinate in color.
TABLE 2.1 Questions to Explore the Possibility of Alcohol Abuse
CAGE questions
Have you ever felt the need to Cut down on your drinking?
Have people Annoyed you by criticizing your drinking?
Have you ever felt Guilty about your drinking?
Have you ever had a morning “Eye-opener” to steady your nerves or get rid of a hangover?
HALT questions
Do you usually drink to get High?
Do you drink Alone?
Do you ever find yourself Looking forward to drinking?
Have you noticed that you are becoming Tolerant to alcohol?
BUMP questions
Have you ever had Blackouts?
Have you ever used alcohol in an Unplanned way (drank more than intended or continued to drink after having enough)?
Do you ever drink for M edicinal reasons (to control anxiety, depression or the “shakes”)?
Do you find yourself Protecting your supply of alcohol (hoarding, buying extra)?
Determining if the patient has ever engaged in risky sexual behavior is sometimes important, and the subject always difficult to broach.
Patients are often less reluctant to discuss the topic than the examiner. Useful opening gambits might include how often and with whom
the patient has sex, whether the patient engages in unprotected sex, or whether the patient has ever had a sexually transmitted disease.
REVIEW OF SYSTEMS

In primary care medicine the review of systems (ROS) is designed in part to detect health problems of which the patient may not complain,
but which nevertheless require attention. In specialty practice, the ROS is done more to detect symptoms involving other systems of
which the patient may not spontaneously complain but that provide clues to the diagnosis of the presenting complaint. Neurologic disease
may cause dysfunction involving many different systems. In patients presenting with neurologic symptoms, a “neurologic review of systems”
is useful after exploring the present illness to uncover relevant neurologic complaints. Some question areas worth probing into are
summarized in Table 2.2. Symptoms of depression are often particularly relevant and are summarized in Table 2.3. A more general ROS may
also reveal important information relevant to the present illness (Table 2.4). Occasional patients have a generally positive ROS, with
complaints in multiple systems out of proportion to any evidence of organic disease. Patients with Briquet syndrome have a somatization
disorder with multiple somatic complaints which they often describe in colorful, exaggerated terms.
The ROS is often done by questionnaire in outpatients. Another efficient method is to do the ROS during the physical examination, asking
about symptoms related to each organ system as it is examined.
TABLE 2.2 A Neurologic System Review; Symptoms Worth Inquiring About in Patients Presenting with Neurologic
Complaints
Any history of seizures or unexplained loss of consciousness
Headache
Vertigo or dizziness
Loss of vision
Diplopia
Difficulty hearing
Tinnitus
Difficulty with speech or swallowing
Weakness, difficulty moving, abnormal movements
Numbness, tingling
Tremor
Problems with gait, balance or coordination
Difficulty with sphincter control or sexual function
Difficulty with thinking or memory
Problems sleeping or excessive sleepiness
Depressive symptoms (Table 2.3)
Modified from: Campbell WW, Pridgeon RM . Practical Primer of Clinical Neurology. Philadelphia: Lippincott Williams and

Wilkins, 2002.
HISTORY IN SOME COMMON CONDITIONS
Some of the important historical features to explore in patients with some common neurologic complaints are summarized in Tables 2.5,
2.6, 2.7, 2.8, 2.9, 2.10, 2.11, 2.12, 2.13. There are too many potential neurologic presenting complaints to cover them all, so these tables
should be regarded only as a starting point and an illustration of the process. Space does not permit an explanation of the differential
diagnostic relevance of
each of these elements of the history. Suffice it to say that each of these elements in the history has significance in ruling in or ruling out
some diagnostic possibility. Such a “list” exists for every complaint in every patient. Learning and refining these lists is the challenge of
medicine.
TABLE 2.3 Some Symptoms Suggesting Depression
Depressed mood, sadness
Unexplained weight gain or loss
Increased or decreased appetite
Sleep disturbance
Lack of energy, tiredness, fatigue
Loss of interest in activities
Anhedonia
Feelings of guilt or worthlessness
Suicidal ideation
Psychomotor agitation or retardation
Sexual dysfunction
Difficulty concentrating or making decisions
Difficulty with memory
Modified from: Campbell WW, Pridgeon RM . Practical Primer of Clinical Neurology. Philadelphia: Lippincott Williams and
Wilkins, 2002.
TABLE 2.4 Items in the Review of Systems of Possible Neurologic Relevance, with Examples of Potentially Related
Neurologic Conditions in Parentheses
General
Weight loss (depression, neoplasia)
Decreased energy level (depression)

Chills/fever (occult infection)
Head
Headaches (many)
Trauma (subdural hematoma)
Eyes
Refractive status; lenses, refractive surgery
Episodic visual loss (amaurosis fugax)
Progressive visual loss (optic neuropathy)
Diplopia (numerous)
Ptosis (myasthenia gravis)
Dry eyes (Sjögren syndrome)
Photosensitivity (migraine)
Eye pain (optic neuritis)
Ears
Hearing loss (acoustic neuroma)
Discharge (cholesteatoma)
Tinnitus (Meniere disease)
Vertigo (vestibulopathy)
Vesicles (H. zoster)
Nose
Anosmia (olfactory groove meningioma)
Discharge (CSF rhinorrhea)
Mouth
Sore tongue (nutritional deficiency)
Neck
Pain (radiculopathy)
Stiffness (meningitis)
Cardiovascular
Heart disease (many)
Claudication (neurogenic vs. vascular)

Hypertension (cerebrovascular disease)
Cardiac arrhythmia (cerebral embolism)
Respiratory
Dyspnea (neuromuscular disease)
Asthma (systemic vaculitis)
Tuberculosis (meningitis)
Gastrointestinal
Appetite change (hypothalamic lesion)
Excessive thirst (diabetes mellitus or insipidus)
Dysphagia (myasthenia)
Constipation (dysautonomia, MNGIE)
Vomiting (increased intracranial pressure)
Hepatitis (vasculitis, cryoglobulinemia)
Genitourinary
Urinary incontinence (neurogenic bladder)
Urinary retention (neurogenic bladder)
Impotence (dysautonomia)
Polyuria (diabetes mellitus or insipidus)
Spontaneous abortion (anticardiolipin syndrome)
Sexually transmitted disease (neurosyphilis)
Pigmenturia (porphyria, rhabdomyolysis)
Menstrual history
Last menstrual period and contraception
Oral contraceptive use (stroke)
Hormone replacement therapy (migraine)
Endocrine
Galactorrhea (pituitary tumor)
Amenorrhea (pituitary insufficiency)
Enlarging hands/feet (acromegaly)
Thyroid disease (many)

Musculoskeletal
Arthritis (connective tissue disease)
Muscle cramps (ALS)
Myalgias (myopathy)
Hematopoetic
Anemia (B
12
deficiency)
DVT (anti-cardiolipin syndrome)
Skin
Rashes (Lyme disease, drug reactions)
Insect bites (Lyme disease, rickettsial infection, tick paralysis)
Birthmarks (phakamotoses)
Psychiatric
Depression (many)
Psychosis (CJD)
Hallucination (Lewy body disease)
Grandiosity (neurosyphilis)
CJD, Creutzfeldt-Jakob disease; DVT, deep venous thrombosis; M NGIE, mitochondrial neurogastrointestinal
encephalomyopathy
TABLE 2.5 Important Historical Points in the Chronic Headache Patient; if the Patient Has More Than One Kind of
Headache, Obtain the Information for Each Type
Location of the pain (e.g., hemicranial, holocranial, occipitonuchal, bandlike)
Pain intensity/severity
Pain quality (e.g., steady, throbbing, stabbing)
Timing, duration, and frequency
Average daily caffeine intake
Average daily analgesic intake (including over-the-counter medications)
Precipitating factors (e.g., alcohol, sleep deprivation, oversleeping, foods, bright light)
Relieving factors (e.g., rest/quiet, dark room, activity, medications)

Response to treatment
Neurologic accompaniments (e.g., numbness, paresthesias, weakness, speech disturbance)
Visual accompaniments (e.g., scintillating scotoma, transient blindness)
Gastrointestinal accompaniments (e.g., nausea, vomiting, anorexia)
Associated symptoms (e.g., photophobia, phonophobia/sonophobia, tearing, nasal stuffiness)
Any history of head trauma
Modified from: Campbell WW, Pridgeon RM . Practical Primer of Clinical Neurology. Philadelphia: Lippincott Williams and
Wilkins, 2002.
For example, Table 2.5 lists some of the specific important historical points helpful in evaluating the chronic headache patient. The
following features are general rules and guidelines, not absolutes. Patients with migraine tend to have unilateral hemicranial or
orbitofrontal throbbing pain associated with GI upset. Those suffering from migraine with aura (classical migraine) have visual or neurologic
accompaniments. Patients usually seek relief by lying quietly in a dark, quiet environment. Patients with cluster headache tend to have
unilateral nonpulsatile orbitofrontal pain with no visual, GI, or neurologic accompaniments and tend to get some relief by moving about.
Patients with tension or muscle contraction headaches tend to have nonpulsatile pain which is bandlike or occipitonuchal in distribution,
and unaccompanied by visual, neurological, or GI upset.
Table 2.6 lists some of the important elements in the history in patients with neck and arm pain. The primary differential diagnosis is usually
between cervical radiculopathy and musculoskeletal conditions such as bursitis, tendinitis, impingement syndrome, and myofascial pain.
Patients with a cervical disc usually have pain primarily in the neck, trapezius ridge, and upper shoulder region. Patients with cervical
myofascial pain have pain in the same general distribution. Radiculopathy patients may have pain referred to the pectoral or periscapular
regions, which is unusual in myofascial pain. Radiculopathy patients may have pain radiating in a radicular distribution down the arm. Pain
radiating below the elbow usually means radiculopathy. Patients with radiculopathy have pain on movement of the neck; those with
shoulder pathology have pain on movement of the shoulder. Patients with radiculopathy may have weakness or sensory symptoms in the
involved extremity.
Tables 2.7, 2.8, 2.9, 2.10, 2.11, 2.12 and 2.13 summarize some important historical particulars to consider in some of the other complaints
frequently encountered in an outpatient setting.
TABLE 2.6 Important Historical Points in the Patient with Neck and Arm Pain; the Differential Diagnosis Is Most
Often Between Radiculopathy and Musculoskeletal Pain
Onset and duration (acute, subacute, chronic)
Pain intensity
Any history of injury

Any history of preceding viral infection or immunization
Any past history of disc herniation, disc surgery, or previous episodes of neck or arm pain
Location of the worst pain (e.g., neck, arm, shoulder)
Pain radiation pattern, if any (e.g., to shoulder, arm, pectoral region, periscapular region)
Relation of pain to neck movement
Relation of pain to arm and shoulder movement
Relieving factors
Any exacerbation with coughing, sneezing, straining at stool
Any weakness of the arm or hand
Any numbness, paresthesias, or dysesthesias of the arm or hand
Any associated leg weakness or bowel, bladder, or sexual dysfunction suggesting spinal cord compression
Modified from: Campbell WW, Pridgeon RM . Practical Primer of Clinical Neurology. Philadelphia: Lippincott Williams and
Wilkins, 2002.
TABLE 2.7 Important Historical Points in the Patient with Back and Leg Pain; the Differential Diagnosis Is Most
Often, as with Neck and Arm Pain, Between Radiculopathy and Musculoskeletal Pain
Onset and duration (acute, subacute, chronic)
Pain intensity
Any history of injury
Any past history of disc herniation, disc surgery, or previous episodes of back/leg pain
Location of the worst pain (e.g., back, buttock, hip, leg)
Pain radiation pattern, if any (e.g., to buttock, thigh, leg, or foot)
Relation of pain to body position (e.g., standing, sitting, lying down)
Relation of pain to activity and movement (bending, stooping, leg motion)
Any exacerbation with coughing, sneezing, straining at stool
Any weakness of the leg, foot, or toes
Any numbness, paresthesias, or dysesthesias of the leg or foot
Relieving factors
Any associated bowel, bladder, or sexual dysfunction suggesting cauda equina compression